1. Field of the Invention
The invention relates to extraction techniques and more particularly to a method of making longan seed extract.
2. Description of the Related Art
(1) Inflammation is part of the complex biological response of vascular tissues to harmful stimuli, such as pathogens, damaged cells, or irritants. Inflammation is a protective attempt by the organism to remove the injurious stimuli and to initiate the healing process. Inflammation is not a synonym for infection, even in cases where inflammation is caused by infection. Although infection is caused by a microorganism, inflammation is one of the responses of the organism to the pathogen. However, inflammation is a stereotyped response, and therefore it is considered as a mechanism of innate immunity. Contents of inflammation comprise nitric oxide (NO), tumor necrosis factor (TNF), interleukin (IL), granulocyte colony stimulating factor (G-CSF), monocyte colony stimulating factor (M-CSF), granulocyte-monocyte colony stimulating factor (GM-CSF), and lymphotoxini (LT) such as TNF-α and TNF-β.
Without inflammation, wounds and infections would never heal. Similarly, progressive destruction of the tissue would compromise the survival of the organism. However, chronic inflammation can also lead to a host of diseases, such as hay fever, periodontitis, atherosclerosis, and rheumatoid arthritis. It is for that reason that inflammation is normally closely regulated by the body.
Typically, antibiotics, non-steroidal anti-inflammation drugs (NSAIDs), and anti-histamine drugs are used to treat inflammation and they improve symptoms. However, side effects are also reported.
(2) Gout is a medical condition usually characterized by recurrent attacks of acute inflammatory arthritis, e.g., a red, tender, hot, swollen joint. Goat can be hypercuricemia, recurrent acute monoarthrities, and tophi. Gouty nephropathy is the symptom of serious goat. The metatarsal-phalangeal joint at the base of the big toe is the most commonly affected. However, it may also present as tophi, kidney stones, or urate nephropathy. It is caused by elevated levels of uric acid in the blood which crystallize and are deposited in joints, tendons, and surrounding tissues.
Hypercuricemia is the main cause of gout. About 5-18.8% patients suffering hypercuricemia may have gout in the end period. It is fatal in some cases.
Uricase differential spectrophotometric method can be used to cure hyperuricemia. Hyperuricemia is a level of uric acid in the blood that is abnormally high. In humans, the upper end of the normal range is 360 μmol/L (6 mg/dL) for women and 400 μmol/L (6.8 mg/dL) for men. Many factors contribute to hyperuricemia including genetics, insulin resistance, hypertension, renal insufficiency, obesity, diet, use of diuretics, and consumption of alcoholic beverages.
Hyperuricemia has four stages including asymptomatic hyperuricemia, acute gouty arthritis, inter-critical gout, and chronic tophaceous gout.
Diagnosis is confirmed clinically by the visualization of the characteristic crystals (e.g., monosodium urate crystal) in joint fluid. Shown negative birefringent means gout symptom. Other parts of a patient including toes, feet, and ankles can be also observed for gout symptom.
Treatment with steroids or colchicine improves gout symptoms. Once the acute attack has subsided, levels of uric acid are usually lowered via lifestyle changes, and in those with frequent attacks allopurinol or probenecid provide long-term prevention.
Precipitation of uric acid crystals, and conversely their dissolution, is known to be dependent on the concentration of uric acid in solution, pH, sodium concentration, and temperature. Established treatments address these parameters.
Uricosuric agents are substances that increase the excretion of uric acid in the urine, thus reducing the concentration of uric acid in blood plasma. In general, this effect is achieved by action on the proximal tubule. Drugs that reduce blood uric acid are not all uricosurics. Blood uric acid can be reduced by administered uricosuric agents for seven to ten days gradually increased in amount. Other drugs such as probenecid and benzbromarone can also be used.
Treatment with xanthine oxidase inhibitor, allopurinol, hypoxanthine, and xanthine oxidase improves symptoms. Also, mercaptopurine or azathioprine can be used to treat gout but caution should be taken due to its side effects.
(3) Wound healing is an intricate process in which the skin repairs itself after injury. In normal skin, the epidermis (i.e., outermost layer) and dermis (i.e., inner or deeper layer) exists in a steady-state equilibrium, forming a protective barrier against the external environment. Once the protective barrier is broken, the normal process of wound healing is immediately set in motion. The classic model of wound healing is divided into four sequential phases: hemostasis, inflammatory, proliferative, and remodeling. Upon injury to the skin, a set of complex biochemical events takes place in a closely orchestrated cascade to repair the damage. Within minutes post-injury, platelets aggregate at the injury site to form a fibrin clot. This clot acts to control active bleeding.
Growth factors related to wound healing include fibroblast growth factor 2 (FGF2), platelet-derived growth factor (PDFG), epidermal growth factor (EFG), keratinocyte growth factor (KGF), transforming growth factor-α (TGF-α), transforming growth factor-β (TGF-β), and vascular endothelial growth factor (VEGF). These growth factors including PDFG, EFG, TGF-β, and VEFG are secreted by cells. Further, PDGF can absorb macrophages and fibroblasts and facilitates matrix protein growth. EGF can autocrine for growth. TGF-β can facilitate fibroblasts growth. VEGF can facilitate proangiogenic matrix growth and accelerate monocyte movement. These factors are closely related to wound healing.
In the inflammatory phase, bacteria and debris are phagocytosed and removed, and factors are released that cause the migration and division of cells involved in the proliferative phase. The proliferative phase is characterized by angiogenesis, collagen deposition, granulation tissue formation, epithelialization, and wound contraction. In angiogenesis, new blood vessels are formed by vascular endothelial cells. In fibroplasia and granulation tissue formation, fibroblasts grow and form a new, provisional extracellular matrix by excreting collagen and fibronectin.
The invention discussed below is novel and nonobvious as far as the present inventor is aware.